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PubMed1984

Effects of ethanol and acetaldehyde on cultured rabbit aortic myocytes and human platelets in vitro.

The recently reported finding that a moderate alcohol consumption may lower the risk of cardiovascular disease prompted a study of the effects of ethanol and acetaldehyde on proliferation, viability and collagen secretion of rabbit aortic myocytes in culture and on the spontaneous efflux reaction of human platelets in vitro. Ethanol had no effects on any of the systems and acetaldehyde did not influence platelets significantly. Fifty mumol 1(-1) acetaldehyde diminished the proliferation and collagen secretion of arterial myocytes by 20% (P less than 0.01) and 100 mumol 1(-1) acetaldehyde by 39% (P less than 0.001) without affecting cell mass or cell death. A metabolic degradation, and some evaporation, of acetaldehyde was taking place and 50 mumol 1(-1) acetaldehyde was halved after approximately 2 h. The more 'physiological' concentration of acetaldehyde (5 mumol 1(-1] influenced cell proliferation significantly (P less than 0.001) if the concentration was restored by 6-h intervals and the incubation time increased from 24 to 48 h. The weak aldehydedehydrogenase inhibitor chlorpropamide did not accentuate the effects of acetaldehyde.

Acetaldehyde↗
PubMed1996

Changes in prescribing patterns of oral hypoglycaemics in elderly patients, over a period of 10 years: matching with general practitioners' perceptions of their own prescribing.

A 10-year hospital admissions database had demonstrated a steep decline in the prescribing of chlorpropamide, and to a lesser degree, of glibenclamide, with tolbutamide, metformin and the most recently introduced oral hypoglycaemic, gliclazide, maintaining relatively uniform levels. Glipizide was the most popular emerging agent. Interviews with 20 general practitioners (GPs) revealed that 55% had a definite first choice agent with a priority order of gliclazide, tolbutamide and glibenclamide. For the remaining GPs without a sole preference, gliclazide (30%), glipizide (30%) and glibenclamide (20%) featured as their most commonly prescribed agents.

Administration, Oral↗
PubMed1989

Proliferative diabetic retinopathy in a patient with maturity-onset diabetes of the young (MODY).

Maturity-onset diabetes of the young (MODY) has been described as being characteristically free from severe complications. This has led to speculation that the type of diabetes may be important in the pathogenesis of complications in diabetes. We report a case of classical MODY in which severe proliferative diabetic retinopathy developed. The retinopathy was detected shortly after the diagnosis of diabetes was made when the patient was 32 years old, and did not progress subsequently. No further complications developed during the subsequent 29 years in which normal postprandial plasma glucose levels were maintained with chlorpropamide therapy (mean 4.7, range 4.1-6.0 mmol I-1). This case demonstrates that severe retinopathy can occur in MODY and we suggest that in this patient there may have been a period of hyperglycaemia prior to diagnosis which was sufficient to lead to the microvascular complication.

Adolescent↗
PubMed2005

Changing patterns of primary care for diabetes in Trinidad and Tobago over 10 years.

OBJECTIVE: To evaluate standards of preventive medical care for Type 2 diabetes in the context of high prevalence and limited resources. METHODS: Surveys of records for diabetic subjects attending 23 government primary care health centres in Trinidad and Tobago in 2003 and 1998 and nine health centres in 1993. Records were compared by study year for blood glucose and blood pressure, surveillance for complications, appropriate management advice and drug prescriptions. Relevant interventions included new clinical guidelines, training workshops for clinical staff and reports to the Ministry of Health. During this time, investment in primary care increased in the context of health sector reform policies and a favourable macroeconomic environment. RESULTS: Comparing 1993 with 2003, the proportion with a blood glucose test in the past 12 months increased from 33% to 91%, urea or creatinine ever recorded increased from 14% to 61%, diet advice recorded in the first 12 months of follow-up from 35% to 67%, exercise advice from 3% to 61%. The proportion prescribed metformin increased from 25% to 65%, while chlorpropamide decreased from 48% to 0%. The proportion of all subjects treated with antihypertensive drugs increased from 49% to 70%, and the proportion of treated patients prescribed angiotensin-converting enzyme inhibitors increased from 8% to 72%. Most recent ever records of blood glucose, blood pressure and body weight showed no decrease. CONCLUSIONS: Repeated surveillance of processes of care provided information to stimulate and plan change. Process changes were associated with intervention at several levels and increased availability of resources.

Attitude of Health Personnel↗
PubMed1991

The binding site for [3H]glibenclamide in the rat cerebral cortex does not recognize K-channel agonists or antagonists other than sulphonylureas.

The binding of the potent oral antidiabetic sulphonylurea [3H]glibenclamide was studied in rat cerebral cortex membranes. A single population of high affinity and saturable binding sites with equilibrium constants, Kd = 0.2 +/- 0.06 nM and Bmax = 58.6 +/- 6.2 fmol/mg protein was found. Specific [3H]glibenclamide binding to rat cerebral cortex membranes was inhibited by glibenclamide and other sulphonylureas, glibenclamide being the most potent drug and the sulphonylurea of the second generation chlorpropamide the least potent. This observation suggests that this site may be related to the hypoglycaemic properties of sulphonylureas and possibly to their interaction with ATP-sensitive K(+)-channel. Nevertheless, other non-selective K(+)-channel antagonists such as TEA, 4-aminopyridine, quinine, quinidine or apamin failed to interact with this site (IC50 greater than 100 microM). Similarly, both non-selective K(+)-channel agonists such as cromakalim, pinacidil or minoxidil as well as the pancreatic ATP-sensitive K(+)-channel agonist diazoxide failed to interact with this site. It may thus be concluded that this site, under the present experimental conditions, represents a drug specific recognition site which may be coupled to the hypoglycaemic activity of sulphonylureas, possibly on a particulate ATP-dependent K(+)-channel.

Animals↗
PubMed1966

Application of newer concepts in diabetes.

The changing definition of diabetes, brought up to date, includes the concepts of premellitus as well as mellitus, and of an enzymatically impaired or otherwise ineffective insulin as the possible cause of the full syndrome. Another current concept holds that an increased amount of this lipogenically active but glycolytically impaired insulin is the mechanism producing obesity in diabetes as a premellitic sign. Despite changed concepts the importance and effectiveness of prophylactic weight control in the premellitic stage, and as the fundamental treatment in all stages of obesity-diabetes remains the same. The order of preference in the addition of specific drugs to the dietary treatment of obesity-diabetes is anorexigenic agents, phenformin, single sulfonylureas, and combined chlorpropamide-phenformin. Insulin is the therapy of last resort in this usually mild form of diabetes. There is great potential usefulness for oral hypoglycemic combination therapy (with steroids temporarily if necessary) as a replacement for insulin in the treatment of immunologically-produced insulin resistance.

Blood Glucose↗
PubMed1986

The mechanism of alcohol intolerance produced by various therapeutic agents.

According to clinical reports, several therapeutic agents produce ethanol intolerance, which is often referred as disulfiram reaction. The mechanism of this manifestation was investigated in the Wistar rat, by measuring the alcohol and aldehyde dehydrogenases (ADH, ALDH) of the liver and the brain after subacute administration of chloramphenicol (100 mg/kg X 4, intraperitoneally), chlorpropamide (80 mg/kg X 4, intraperitoneally), disulfiram (150 mg/kg X 4, intraperitoneally), griseofulvin (100 mg/kg X 4, intraperitoneally), isoniazid (200 mg/kg X 4, intraperitoneally), metronidazole (200 mg/kg X 4, intraperitoneally), and procarbazine (100 mg/kg X 4, intraperitoneally). All substances tested decrease the activity of the low-Km ALDH in the brain, with the exception of griseofulvin. The hepatic low-Km enzyme is also inhibited, with the exception of griseofulvin and metronidazole. The high-Km ALDH responds in an inconsistent way, while ADH is not affected at all. The results suggest that the so-called "disulfiram-reaction" is mediated mainly, but not exclusively, by inhibition of the low-Km ALDH.

Alcohol Dehydrogenase↗
PubMed1996

Phototoxicity due to sulphonamide derived oral antidiabetics and diuretics: investigations in a cell culture model.

A number of sulphonamide-derived oral antidiabetics (chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide and tolbutamide) and diuretics (bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chloratalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, piretanide, polythiazide, trichlormethiazide and xipamide) were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzyl-hydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, piretanide, polythiazide and trichlormethiazide. Bendroflumethiazide was phototoxic at 5x10(-5) M and higher concentrations, bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at 2.5x10(-4) M and higher concentrations, and the oral antidiabetics glibenclamide and gliquidone as well as the diuretics butizide, hydrochlorothiazide, piretanide, polythiazide and trichlormethiazide were phototoxic at 5(-4) M and higher concentrations. Electron microscopic investigations showed swelling of mitochondria and endoplasmic reticulum as well as aggregation of euchromatin when the cells were irradiated in the presence of photosensitizers.

Administration, Oral↗
PubMed1985

Similarities in the release rates of different drugs from polyethylene glycol 6000 solid dispersions.

The dissolution rates (mg min-1) of 10 drugs, solid dispersed by fusion in polyethylene glycol 6000 (PEG 6000) have been examined by rotating disc methodology. The dispersions generally displayed release rates which were linearly dependent upon the drug concentration (% drug) at high polymer content. However the range over which this linearity was encountered varied unduly, e.g. 0-2% for phenylbutazone and 0-15% for paracetamol. The slope of this line (mean value: 0.451 mg min-1 % -1) was statistically the same for nine of the drugs studied, the exception being griseofulvin which did not form a true solid dispersion but was a microcrystalline dispersion of the drug within the PEG. During fusion, chain scission of the PEG 6000 occurred in the presence of several drugs. PEG 6000 was incompatible with disulfiram, frusemide, chlorothiazide and chlorpropamide.

Chemistry, Pharmaceutical↗
PubMed1985

Association of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness. The Wolfram or DIDMOAD syndrome.

Seven patients with a rare syndrome of diabetes insipidus (DI), diabetes mellitus (DM), optic atrophy (OA), neurosensory deafness (D), atony of the urinary tract, and other abnormalities (Wolfram or DIDMOAD syndrome) are reported. Of the seven patients, three siblings were followed up for 10-17 years. All seven patients had diabetes mellitus and optic atrophy; six had diabetes insipidus; and in the four patients investigated there was dilatation of the urinary tract. The severity of diabetes varied, and all required insulin for control of the hyperglycaemia. In one patient the course of the disease simulated maturity onset diabetes of the young; another presented with ketoacidosis; but none had haplotypes usually associated with insulin dependent diabetes mellitus. The diabetes insipidus responded to chlorpropamide, suggesting partial antidiuretic hormone deficiency. Onset of optic atrophy and loss of vision occurred relatively late and progressed slowly, although in one patient there was a rapid deterioration in visual acuity. Deafness was mild, of late onset, and of sensorineural origin. A degenerative process affecting the central and peripheral nervous system can explain all the manifestations of the syndrome except diabetes mellitus. The pathogenesis of the diabetes mellitus remains obscure.

Child↗
PubMed1977

Symptomatic hyponatraemia associated with tolbutamide therapy.

A case of hyponatraemic coma occurring in a patient with diabetes mellitus treated with tolbutamide is described. Although chlorpropamide is known to cause water retention in some circumstances, this is a less well recognized complication of tolbutamide therapy.

Diabetes Mellitus↗
PubMed1981

Intrahepatic cholestasis and cutaneous bullae associated with glibenclamide therapy.

Intrahepatic cholestasis and cutaneous bullae associated with glibenclamide therapy are described in a 61-year-old diabetic patient who presented wit hypoglycaemic coma. These features have not previously been reported as side effects of glibenclamide therapy, but intrahepatic cholestasis may occur with chlorpropamide, a similar sulphonylurea agent. The mechanism of this cholestasis is not clear at present.

Blister↗
PubMed1989

Drug-induced acute liver disease.

Fifty-three patients with drug-induced acute liver disease are reported. There were 35 females and 18 males with a mean age of 41 years. All but one patient had jaundice or hyperbilirubinaemia and 51 had abnormal liver enzymes. Histologically 38 patients (72%) had cholestatic injury while 15 had cytotoxic parenchymal damage. Methyldopa, chlorpropamide, chlorpromazine, halothane and the contraceptive pill accounted for 60% of cases. Fifty-one patients recovered after drug withdrawal while 2 died of hepatic failure. Drug-induced liver injury must be considered in patients presenting with evidence of hepatic disease as the majority will recover on withdrawal.

Acute Disease↗
PubMed1983

Hypoglycemic effect of guava juice in mice and human subjects.

Guava is a plentiful fruit in Taiwan and it was taken from the plants of Psidium guajava Linn. (Myrtaceae). According to the folklore in Chinese Medicine, gauva was useful in the treatment of diabetes mellitus. In the present study, acute i.p. treatment with 1 g/kg guava juice produced a marked hypoglycemic action in normal and alloxan-treated diabetic mice. Although effective duration of guava is more transient and it is less potent than chlorpropamide and metformin, blood glucose lowering effect of guava also can be obtained by oral administration in maturity-onset diabetic and healthy volunteers. Thus, it is suggested that guava may be employed to improve and/or prevent the disease of diabetes mellitus.

Adolescent↗
PubMed1994

Antagonism of eicosanoid-induced contraction of rat aorta by sulphonylureas.

Glibenclamide and other sulphonylureas are extensively used as specific blockers for ATP-dependent potassium channels in vascular smooth muscle. However, glibenclamide has recently been shown to inhibit actions of some prostanoids in vascular smooth muscle. We extend our previous study by examining the relaxant actions of five different sulphonylureas in rat aorta. The inhibitory effects of sulphonylureas on the contractions induced by prostaglandins F2 alpha, E2 and D2, norepinephrine, 5-hydroxytryptamine (5-HT) or potassium chloride (KCl) were examined. Glibenclamide significantly inhibited the contractions produced by prostaglandins F2 alpha, E2 and D2 but was without effect on responses to norepinephrine, 5-HT or KCl. Glimepiride produced significant attenuation of the responses to all agents tested (5-HT, norepinephrine, KCl), although the inhibition of the responses to prostaglandin F2 alpha was most pronounced. Glipizide and tolbutamide had activities similar to that of glibenclamide, while chlorpropamide was devoid of any antagonist action in rat aorta. In rat aorta precontracted with norepinephrine, glibenclamide inhibited the relaxant responses to lemakalim and pinacidil. Thus, in addition to the effect on ATP-dependent potassium channels, glibenclamide inhibits responses to prostaglandins F2 alpha, E2 and D2 but not to other agents. This effect is shared by glimepiride, tolbutamide and glipizide.

Animals↗
PubMed1988

Effects of sulfonylureas on the synthesis and secretion of plasminogen activator from bovine aortic endothelial cells.

The effects of sulfonylureas on the production of plasminogen activator (PA) and antiactivator (PAI) were investigated using bovine aortic endothelial cells. All compounds studied stimulated PA release (1.3- to 5.2-fold), with glipizide being the most potent, followed by tolazamide, chlorpropamide, and tolbutamide, in that order, while glyburide was the least effective. Both tissue-type and urokinase-type PA production was enhanced. Studies using metabolic inhibitors indicated that both RNA and protein syntheses are required for the sulfonylurea-mediated stimulation of PA release. In addition to continuous release of the two PAs, there was also a continuous release of a single PAI, which did not show an increase after the sulfonylureas. These results suggest that, in addition to their beneficial effects in the treatment of diabetes mellitus, some sulfonylurea compounds may also have significant thrombolytic effects. These results also suggest that pharmacological enhancement of PA production by vascular endothelial cells may be a promising antithrombotic mechanism.

Animals↗
PubMed1988

Neonatal diabetes mellitus in first cousins.

The cases of two first cousins with neonatal diabetes mellitus are presented in this report. In one child the condition was transient, whereas the other has permanent diabetes mellitus. It seems unlikely that the difference in outcome was related to the degree of diabetic control early in the course of the disorder. The possibility of genetic influence in the etiology of neonatal diabetes is stressed. Chlorpropamide was not useful in curing neonatal diabetes mellitus in one case.

Blood Glucose↗
PubMed1990

Symptomatic hypoglycemia secondary to a glipizide-trimethoprim/sulfamethoxazole drug interaction.

Sulfonamides have been reported to augment the hypoglycemic effects of chlorpropamide, glyburide, and tolbutamide. This case report is the first to describe a possible interaction with glipizide. An 83-year-old man receiving glipizide 10 mg bid developed symptomatic hypoglycemia within three days of adding trimethoprim/sulfamethoxazole (TMP/SMX) to his regimen. All other factors, including laboratory data, dietary intake, activity level, and concurrent use of other medications, were stable and noncontributory. This patient may have been at increased risk for this interaction secondary to his age and history of alcohol abuse. The mechanism of the interaction is probably inhibition of glipizide metabolism rather than protein-binding displacement. This case suggests that, when TMP/SMX is combined with glipizide, patients should be closely monitored, especially those at high risk for hypoglycemia.

Aged↗